AJP - Heart and Circulatory Physiology, Vol 249, Issue 4 715-H722, Copyright © 1985 by American Physiological Society
Increased myocardial contractility during endotoxin shock in dogs
P. M. Kober, J. X. Thomas Jr and R. M. Raymond
The slope of the left ventricular (LV) end-systolic pressure-diameter
relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized
dogs before and after endotoxin administration. A lead II
electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and
LV minor axis diameter were measured. After control measurements were
taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n =
5) or an equivalent volume of saline (n = 4). Control dogs were followed
for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min).
There were no significant changes in Ees in control dogs (17 +/- 3
mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly
increased in endotoxic dogs even into the late stages of shock (41 +/- 11
mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall
significantly below control (11 +/- 2 mmHg/mm, P less than 0.05).
End-diastolic diameter decreased following endotoxin administration (P less
than 0.05) but returned toward control by the terminal stage. Peak + LV
dP/dt was depressed following endotoxin injection. Myocardial contractility
was not depressed except as a terminal event. Early depression of
cardiovascular performance in endotoxic dogs was therefore due to decreased
preload and not cardiac dysfunction.
